To study the inhibitory effect of new retinoid 4-acetamidophenyl retinoate (4-APR) on the reconstituted basement membrane invasion by B16-F10 mouse melanoma cells and its mechanism.

Chemotherapy is one of important adjuvant therapies for patients with pancreatic adenocarcinoma, but the mechamism 5-FU and MMC distributed over the pancreas is not known at home and abroad. Based on determining the ratio of the concentration of several kinds of antibioticsin plasma and pancreatic juice, we used fourteen dogs to study the distribution and the relationship of agents in plasma and pancreatic juice after giving 5-FU and MMC intravenously. At the same time, we observed some patients who received Whipple's operation. The results showed that 5-FU and MMC in plasma can penetrate the pancreatic tissue and cross the blood-pancreatic juice barrier (BPJB). Both agents suitable for the adjuvant chemotherapy of pancreatic adenocarcinoma.

The effects of intravenous injection of cisplatin (CDDP) and the incubated with CDDP in vitro on the epitopes and cytotoxicity of TIL obtained from eight colorectal tumor patients were detected respectively by flow cytometer. There was a significant increase in CD3+/CD8+ subset in TIL in patients receiving intravenous injection of CDDP. And the cytotoxicity of these TILs increased significantly. The cytotoxities were positively correlated with the amount of CD3+/CD8+ subset in TIL. Raji cells incubated with CDDP in vitro showed increased susceptibility to TIL induced lysis.

This research was to observe the effects of lithium chloride (LiCl) and Harringtonine (HT) on the proliferation and differentiation of HL-60 leukemia cells. The results obtained by liquid suspension culture, semi-solid colony culture and 3H-TdR incorporation into HL-60 cells indicated that different concentrations of LiCl (5-20 mmol/L) and HT (10(-8)-10(-5)mol/L) exerted the inhibitory effects in a dose-dependent manner on HL-60 cell proliferation respectively. When LiCl (10 mmol/L) and HT (10(-7) mol/L) were added together in the liquid culture or semi-solid culture of HL-60 cells, they showed much greater inhibitory effect than that by each agent separately. It was discovered that there was induction of the differentiation of HL-60 cells by lithium and HT and the induction of HL-60 cells differentiation by HT was markedly enhanced by the addition of low concentration of lithium. This work also showed that by treating HL-60 cells with lithium and HT, the expression of the c-myc proto-oncogene was markedly decreased as measured by RT/PCR-mRNA (P < 0.01). These findings provide some evidence of the mechanismcausing leukemic change and of the potential use of lithium and HT in the treatment of leukemia and in vitro purging of leukemic cells for autologous bone marrow transplantation.

Changes of [Ca2+]i in CCL229 cells induced by retionoic acid (RA), 1,25(OH)2VD3 and PMA were measured by spectrofluorometry. The effects of endoplasmic reticulum (ER)-specific Ca(2+)-ATPase inhibitor thapsigargin (TG) and IP3 receptor inhibitor heparin on RA-induced changes of [Ca2+]i were observed and the relationship between RA-induced changes of [Ca2+]i and ER was also investigated. The results showed that [Ca2+]i increased markedly in several seconds after treated by RA and 1,25(OH)2VD3. When cells were pretreated with EGTA and verapamil (Ca2+ entry blocker drug), TG could not inhibit RA-stimulated Ca2+ release from intracellular calcium pools and TG could increase [Ca2+]i after pretreated by RA. In addition, heparin could not completely inhibit RA-induced [Ca2+]i increase. The results suggest that RA might stimulate IP3-sensitive pool or IP3-insensitive pool on ER to increase [Ca2+]i, or there might be RA-sensitive calcium pools except ER in cells.

To explore the biological effect of Q-wave millimeter microwave (QWMM).

To study the relationship between in vitro chemosensitivity of human breast cancer to MDR related drugs and expression of mdr-1 gene.

It was reported that sodium thiosulfate (STS) was contributed to antivomiting effect in 20 transarterial chemotherapic patients. The antitumor sensitivity of STS (< 500 micrograms/ml) adjuncting to the ADM, MMC, CDDP and other four agens (1 x PPC/ml) individually on two tumor cells studied by MTT test in vitro and no antitumor activity of adjuvant of STS were obviously obliterated (P > 0.05) except for CDDP clinically, to comparing the adjuncting effects of STS (iv. 30 min ahead) or metochlopramidum (im. 30 min ahead) to ADM, MMC and CDDP on HCC (40 cases), the degrees of vomiting in hepatoma patient after transcatheter arterial chemoem bolization with ADM, MMC and CDDP were statisticaly analysec. It have been proven that STS was contributed to the low incidence of vomiting and superior to metocloe pramidum, without worsening of the chemotherapy of HCC. It is worth futher studying adjuvant STS to other antitumor drugs and exploring potential application of chematherapy in cancer.

The role of genistein in the effect of growth factors (KGF and EGF) on the growth of HPV 16 DNA-immortalized human cervical epithelial cells (HCE 16/3 cells) was studied.

To study the antitumor and immunological activities of oxalysine (OXL).

Considerable evidence has showed that apoptosis is involved in both cancer development and inhibition. A new assay (terminal deoxynucleotidyl transferase assay, TdT assay) was recently reported to have advantages in the detection of apoptosis. In this study, this assay was used to investigate antitumor drug-induced apoptosis in human cancer cells.

To elucidate the pattern of chemotherapy drugs induced apoptosis and its role in chemotherapy of acute leukemia.

To investigate the mechanism by which taxol induces apoptosis in human breast cancer cells.

To study the biological significance of Grp94 deleted product (Grp94 beta) expressed in human colorectal carcinoma cells.

We detected the antiproliferative effect with MTT test and investigated the changes in biological properties, cytomorphology and ultrastructure through cytopathology and electronic microscopy. Cell growth of JF-305 was inhibited by all-trans retinoic acid (ATRA). The maximal inhibitory rate was 34.7%. The number of proliferative cells reduced (P < 0.01). Cell metabolism slowed down, secretory functions recovered, and malignant degree decreased. ATRA can inhibit the proliferation and induce the differentiation of human pancreatic adenocarcinoma JF-305 cells.

Proliferation, cell cycle, total amount of DNA, area of cell nucleus, as well as epidermal growth factor receptors (EGFR) and expression of oncogene C-erbB2 mRNA of Chinese breast cancer cell line (BCaP-37) after being treated with kappa-selenocarrageenan were determined by cell culture technique, image cytometry (ICM) and northern blot to explore its anti-tumor mechanism. Results revealed 3.0-120 mg/L selenocarrageenan could inhibit proliferation of BCaP-37, with a response of time and dose dependence. The areas of nuclei were significantly lower with ICM in cells treated with 15 or 60 mg/L selenocarrageenan for four days than those in controls (P < 0.01). Levels of EGFR and expression of C-erbB2 mRNA were significantly inhibited in cells treated with 60 mg/L selenocarrageenan. It suggests that selenocarrageenan can inhibit proliferation of breast cancer cells through regulation of the levels of EGFR and expression of C-erbB2 mRNA.

To assess the feasibility of delivering liposomal adriamycin (lipo-ADM) to the regional lymph nodes via intralymphatic infusion in a rabbits model.

For further investigating the efficacy and side effects of meisoindico.

Human lung cancer leads the mortality of cancers and the chemotherapy is often uneffective because of drug resistance. In order to study the role of mdr-1 gene in resistant lung cancer, the fully length mdr-1 cDNA was transferred into a sensitive lung cancer cell line GLC. The mdr-1 cDNA was constructed in a retroviral vector, pDORneo. The transfection of recombinant plasmid was carried out by lipofectin. Supernatant containing infective viruses derived from a G418 resistant clone of package cell PA317 was used to infect GLC cell which is sensitive to chemotherapeutic agents. After G418 and adriamycine selections, three P-glycoprotein positive clones were isolated and the integration of mdr-1 cDNA was demonstrated by PCR of genomic DNA. The relative resistance of 3 clones to adriamycine as and elevated by 5.4, 6.0 respectively 7.8 times compared with the untransfected cell and the transcription of mdr-1 gene in these transfected cells as obviously enhanced by in situ hybridization. This results suggest that the mdr-1 gene plays a role in increasing drug resistance of human lung cancer.